The hypothesis to be tested is that changes in noncontractile structural elements of the arterial wall cause or maintain the increased resistance to blood flow and the high arterial pressure in hypertension. It is proposed that apparent changes in wall thickness and contractile elements in smooth muscle cells of the arterial wall, and the increased reactivity and resistance of the intact arterial system are caused in part if not entirely by the interaction of a decreased resting distensibility with other properties of the vessel (i.e., length dependent contractile force, sensitivity, and thickness) that are unchanged with hypertension. A possible mechanism for a decreased distensibility without hypertrophy is an increased density of cross-links in collagen and elastin. Mechanical experiments on vessels from perinephritic hypertensive dogs and spontaneously hypertensive rats and from their controls will show a change in the resting stress-strain relation, resting stress relaxation, and the series elastic element stress-strain relation. Since changes in the arterial wall are confined to noncontractile elements quick release experiments will show that no change occurs in the force-velocity relation. Our previous results show no change in the length-active stress relation with hypertension whereas resting distensbility is decreased. Apparent differences in active stress were shown using data from the same experiments. Our finding of a length-dependent sensitivity will be used to show that this relationship interacts with a decreased resting distensibility to cause apparent differences in sensitivty from in vitro experiments. On-line measurement of media thickness and other dimensions with a video dimension analyzer will be used to show that wall thickness/lumen ratio depend on arterial diameter and if any changes occur with hypertension. End effects caused by tethering of the specimen will be eliminated during dynamic experiments with a video dimensional analyzer that monitors the undamaged central portion of the arterial specimen. Mechanical parameters from stress-strain and relaxation experiments can be used in future work to relate mechanisms (i.e., collagen crosslinking and synthesis) to changes in vessel distensibility and viscosity.